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  • Title: Manual and hemispheric asymmetries in the execution of actual and pantomimed prehension.
    Author: Laimgruber K, Goldenberg G, Hermsdörfer J.
    Journal: Neuropsychologia; 2005; 43(5):682-92. PubMed ID: 15721181.
    Abstract:
    Impairments of the ipsilesional hand after brain damage have been reported in goal-directed motor acts and in pantomimes; the relationship between both movement conditions is largely unknown. In the presented study, pantomimed and actual prehension was examined in 29 stroke patients with left brain damage (LBD) or right brain damage (RBD) as well as in 21 control subjects. Kinematic analyses revealed various performance differences between the conditions of movement execution and the subject groups. The differences depended on the hand tested and on the side of the brain lesion. During actual prehension deviations from normal performance were obvious in the peak velocity of the transport component of the movement, which was reduced in RBD patients, and in the duration of the final adjustment phase, which was prolonged in both patient groups. Pantomime changed various features of movement execution. The transport component was particularly altered in the groups performing with the right hand. Hand aperture was significantly smaller during pantomime than during actual movement execution in all groups. However, this effect was particularly obvious in LBD patients, in whom the hand aperture was even completely absent during many of their pantomimes. Actual movement execution immediately preceding the pantomimes did not change the characteristic features of pantomimes. Thus, the cerebral processes for actually executed and pantomimed motor acts differ. Actual movements seem to be governed by external affordances and constraints; whereas, pantomimes may represent a symbolic act. During prehension, differences in grip formation reveal most directly this dichotomy. We argue that the left hemisphere plays a special role in the generation of the symbolic act; a lesion may abolish grip formation and causes the clinical symptom of apraxia.
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